Long-lasting nosocomial persistence of chlorhexidine-resistant Serratia marcescens in a veterinary hospital.

Healthcare-associated infections (HAIs) are often overlooked in veterinary medicine. Serratia marcescens isolates were recovered over a ten-year period from companion animals in a French veterinary hospital. The pets were sampled either for diagnostic purposes or to monitor colonization. A retrospective study showed that 32 S. marcescens isolates were identified as HAI cases and a further 22 cases were associated with colonization of the surgical site. Two S. marcescens lineages were responsible for two different outbreaks during the study period. Chlorhexidine solution (1%) used to impregnate gauze was found to be the source of the second S. marcescens outbreak and all isolates had high MIC values for chlorhexidine (MIC = 128 mg/L). This study reports, for the first time to our knowledge, the nosocomial spread of chlorhexidine-resistant S. marcescens in a veterinary setting and highlights consequences of the improper use of disinfectants.

The roles of membrane estrogen receptor subtypes in modulating dopamine transporters in PC-12 cells.

The effects of 17beta-estradiol (E(2)) on dopamine (DA) transport could explain gender and life-stage differences in the incidence of some neurological disorders. We tested the effects of E(2) at physiological concentrations on DA efflux in nerve growth factor-differentiated rat pheochromocytoma cells that express estrogen receptors (ER) alpha, ERbeta, and G-protein coupled receptor 30 (GPR30), and DA transporter (DAT). DAT efflux was determined as the transporter-specific loss of (3)H-DA from pre-loaded cells; a 9-15 min 10(-9 )M E(2) treatment caused maximal DA efflux. Such rapid estrogenic action suggests a non-genomic response, and an E(2)-dendrimer conjugate (limited to non-nuclear actions) caused DA efflux within 5 min. Efflux dose-responses for E(2) were non-monotonic, also characteristic of non-genomic estrogenic actions. ERalpha siRNA knockdown abolished E(2)-mediated DA efflux, while ERbeta knockdown did not, and GPR30 knockdown increased E(2)-mediated DA efflux (suggesting GPR30 is inhibitory). Use of ER-selective agonists/antagonists demonstrated that ERalpha is the predominant mediator of E(2)-mediated DA efflux, with inhibitory contributions from GPR30 and ERbeta. E(2) also caused trafficking of ERalpha to the plasma membrane, trafficking of ERbeta away from the plasma membrane, and unchanged membrane GPR30 levels. Therefore, ERalpha is largely responsible for non-genomic estrogenic effects on DAT activity.